HIV-2 is characterized by less efficient transmission through the sexual and vertical routes than HIV-1, and by a slower natural clinical course. Nevertheless, HIV-2 infection eventually leads to AIDS. HIV-2 infection must be distinguished from HIV-1 infection, as HIV-2 is naturally resistant to non-nucleoside reverse transcriptase inhibitors, T20, and some protease inhibitors, and as patient follow-up differs from that of HIV-1 infection.
Compared to HIV-1, HIV-2 is characterized by lower viral replication. In the French ANRS cohort CO5 of HIV-2-infected patients (1009 patients in January 2014), 61% of untreated patients have plasma viral loads below 250 copies/mL (cp/mL). Likewise, in a British study, only 8% of patients with CD4>500 cells/mm3 and 62% of patients with CD4<300 cells/mm3 had detectable viral load, implying that 38% of patients had undetectable viral load in an assay with a quantification limit of 100 copies/ml.
Clinical management of HIV-2 infection is hampered by the lack of validated commercial RNA viral load assays. In-house assays are therefore widely used, such as the assay described by Damond et al. (2005) J. Clin. Microbiol. 43:4234-6 which is used for quantifying the viral load in the French cohort CO5 of HIV-2-infected patients.
However, the ACHIEV2E international collaboration on HIV-2 infection showed that plasma HIV-2 RNA values vary considerably between laboratories. Besides, the high genetic diversity of HIV-2, with 9 groups designated A to I, of which only groups A and B are epidemic, also represents an obstacle to accurate viral load quantification: previous studies have thus shown that group B viruses are particularly difficult to quantify with the current assays. In addition, the current HIV-2 assays also suffer from low sensitivity and accuracy.
It is therefore an object of the invention to overcome these limitations.